Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1997;30:629-631

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lopes, H. F.
Right arrow Articles by Krieger, E. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lopes, H. F.
Right arrow Articles by Krieger, E. M.

(Hypertension. 1997;30:629.)
© 1997 American Heart Association, Inc.


Articles

Lipid Metabolism Alterations in Normotensive Subjects With Positive Family History of Hypertension

Heno Ferreira Lopes; Hélio Bernardes Silva; José Augusto Soares; Barreto Filho; Fernanda Marciano Consolim-Colombo; Dante Marcelo Artigas Giorgi; Eduardo Moacyr Krieger

From the Hypertension Unit, Heart Institute, HCFMUSP, São Paulo, Brazil.

Correspondence to Heno Ferreira Lopes, MD, Hypertension Unit, Heart Institute, Av Dr Eneas de Carvalho Aguiar, 44, 05403-000 São Paulo, Brazil.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Abstract Metabolic abnormalities are usually reported in hypertensive patients. These metabolic alterations seem to begin in childhood. The young offspring of hypertensive parents have not been studied thoroughly for metabolic alterations. The aim of this study was to examine the level of total cholesterol, LDL cholesterol, VLDL cholesterol, HDL cholesterol, uric acid, glycemia, aldosterone, and plasma renin activity in a population of 42 young, slender normotensive subjects with positive family history of hypertension (FH+) or negative family history of hypertension (FH-). Measurements were made in 20 young normotensive subjects (age 21.1±2.2 years, 11 males, 15 white, 5 oriental, body mass index of 22.1±2.3 kg/m2) with FH+ and 22 young normotensive subjects (age 19.9±1.4 years, 17 males, 17 white, 5 oriental, body mass index of 22.1±2.3 kg/m2) with FH-. The total cholesterol (4.47±0.8 versus 3.95±0.6 mmol/L), LDL cholesterol (2.74±0.63 versus 2.36±0.61 mmol/L), VLDL cholesterol (0.5±0.25 versus 0.35±0.09 mmol/L), and triglycerides (2.52±1.26 versus 1.76±0.5 mmol/L) were significantly elevated (P<.05) in the FH+ group compared with the FH- group. The total cholesterol/HDL cholesterol ratio was significantly higher in the group with a positive family history of hypertension (3.75±0.02 versus 3.11±0.02, P<.05). Glycemia was slightly elevated in the FH+ group (2.16±0.29 mmol/L) but was not significantly different from that of the FH- group (2±0.2 mmol/L). Uric acid, plasma renin activity, and aldosterone were similar in both groups. We conclude that young, slender normotensive subjects with a positive history of hypertension show alterations in lipid metabolism, suggesting a positive correlation between lipid metabolism and hypertension heredity.


Key Words: hypertension • blood pressure • lipid metabolism


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Hypertension is frequently accompanied by metabolic disorders such as elevated triglyceride level, low level of HDL cholesterol, increase in LDL cholesterol, and glucose intolerance or insulin resistance.1 Borderline hypertensive subjects when compared with normotensive subjects have higher cholesterol level, higher triglyceride level, lower HDL cholesterol, and higher insulin level.2 DNA familial markers of some lipid abnormalities or hypertension have been described before.3 Lipid abnormalities and hypertension independently or occurring together are important risk factors to the atherosclerosis process, and this process seems to begin early in life, in childhood. Metabolic and endocrine abnormalities (elevated total cholesterol, LDL cholesterol, low HDL cholesterol, and elevated norepinephrine, renin, and insulin) have been observed more frequently in normotensive subjects with a family history of hypertension than in subjects with a negative family history of hypertension,4 5 6 resulting in a positive correlation between lipid metabolism and hypertension heredity. Most of the data involving metabolism and the genetics of hypertension were obtained in adult normotensive subjects and not in children and postpubertal subjects, when hypertension seems to begin. We have previously shown that postpubertal normotensives with a positive family history of hypertension have an elevated casual systolic blood pressure and elevated sustained (1-hour resting period, Finapres, Ohmeda-2300) systolic, mean, and diastolic resting blood pressures, suggesting a permanent abnormality rather than a momentary hyperreactivity producing the increased arterial pressure.7 The aim of this study was to evaluate the metabolic and humoral profile in young, slender normotensive subjects with positive and negative histories of hypertension.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Subjects
Forty-two healthy normotensive medical students were selected for the study. They were considered normotensive when casual blood pressure measured after 10 minutes of rest in sitting position at least two times was <140/90 mm Hg. Arterial blood pressure was measured with a mercury sphygmomanometer, using the disappearance of Korotkoff sounds (phase V) as the criterion for the determination of diastolic blood pressure. Subjects with obesity were excluded; degree of obesity was estimated by determining body mass index. The parents with positive or negative history of hypertension were identified by finding evidence in their medical records of antihypertensive treatment or by direct measurement of parents’ blood pressure. No history of diabetes was detected in the parents. Subjects were subdivided into two groups according to their parents’ blood pressure status: positive family history (FH+) when one or two parents were hypertensive and negative family history (FH-) when both parents were normotensive. The age of the population was limited to 18 to 25 years. The characteristics of the two groups are presented in Table 1, showing that the two groups were similar in regard to age, sex, and race. All participants signed an informed consent approved by the Ethics Committee from the Hospital das Clinicas, São Paulo University.


View this table:
[in this window]
[in a new window]
 
Table 1. Characteristics of Normotensive Subjects With Positive and Negative Family History of Hypertension

Protocol
All subjects reported to our laboratory at approximately 8 AM after an overnight fast. After the subjects rested for 1 hour in a supine position, blood samples were collected for measurement of total cholesterol, HDL cholesterol, LDL cholesterol, VLDL cholesterol, uric acid, triglycerides, glycemia, plasma renin activity, and aldosterone. Total cholesterol level was measured by the CHOD-PAP method and the LDL-cholesterol concentration was calculated indirectly (Friedewald formula). The HDL cholesterol was separated with the phosphotungstic acid/magnesium chloride method. Glucose, triglycerides, and uric acid were measured by the enzymatic colorimetric test (GPO/PAP method). Aldosterone and plasma renin activity were measured by radioimmunoassay.

Statistical Analysis
Statistical analysis was performed with the statistical software SAS/STAT.8 Comparisons between categorical variables were performed with the {chi}2 test. Student’s nonpaired t test was applied for the comparison between two related samples. Values for continuous variables are expressed as mean±SD. A value of P<.05 was the minimal level of statistical significance.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
Table 1 shows that the two groups of youngsters under study did not differ significantly regarding age, sex, race, and body mass index. The mean systolic and diastolic blood pressures were significantly higher in the FH+ than in the FH- group (Table 1). Table 2 shows that mean plasma total cholesterol, LDL cholesterol, VLDL cholesterol, and triglycerides were significantly higher in normotensive subjects with positive history of hypertension than in normotensive subjects without history of hypertension, whereas HDL cholesterol did not differ in either group. In addition, the ratio of total cholesterol to HDL cholesterol was significantly higher in the FH+ than in the FH- group. The uric acid level was similar in the FH+ (0.12±0.03 mmol/L) and FH- (0.12±0.03 mmol/L) groups, respectively. Mean fasting plasma glucose was slightly elevated in the FH+ group (2.16±0.29 mmol/L) but was not significantly different from that of the FH- group (2±0.2 mmol/L, P=NS). The plasma renin activity was not different in the FH+ and FH- groups (1.0±1.0 and 1.0±0.9 ng · mL-1 · h-1, respectively), and aldosterone levels did not differ between FH+ and FH- groups (0.27±0.07 and 0.24±0.09 mmol/L, respectively).


View this table:
[in this window]
[in a new window]
 
Table 2. Plasma Lipid and Glycemia Concentrations in Normotensive Subjects With Positive and Negative Family Histories of Hypertension


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
Metabolic abnormalities and hypertension are frequently associated, and this fact contributes to the development of cardiovascular disease. The metabolic abnormalities seem to develop along with hypertension early in life in subjects with genetic predisposition to hypertension. As we have observed before, young normotensive subjects with a positive family history of hypertension exhibit a sustained elevated blood pressure; they seem to reflect not just a transient blood pressure elevation, but one representing a premature and true increase in blood pressure levels.7 In the present study, the young, lean normotensive subjects with a positive history of hypertension had elevated levels of total cholesterol, LDL cholesterol, VLDL cholesterol, and triglycerides when compared with young, lean normotensives without a history of hypertension. The HDL cholesterol level was not different in the FH+ and FH- groups. The basal glucose was slightly elevated in the FH+ group, but it was not significantly different. These characteristics found in normotensive youngsters with a positive history of hypertension, associated with other abnormalities such as insulin resistance and altered glucose tolerance, are relatively frequent in hypertensive patients.6 9 Adult normotensive patients with a family history of hypertension compared with hypertensive patients with or without a family history of hypertension have a similar metabolic profile.6 Metabolic alterations in offspring of hypertensive subjects have been observed before,5 10 11 but the studies were usually performed in subjects older than in our population, and these subjects were exposed for longer times to environmental factors, which may interfere with the metabolic condition. The metabolic abnormalities observed in this study could possibly contribute to vascular structural and reactivity modification early in life. Lipid metabolism alterations are considered risk factors for coronary artery disease, and subjects with a positive history of hypertension could be more susceptible to hypertension and cardiovascular disease. Therefore, this population deserves special preventive care. Treatment of hypertension usually begins during adulthood, at a time when considerable damage may have already been done to the arterial system, the left ventricle, and perhaps to other organs.12 Consequently, it is convenient to identify individual children who are at high risk for cardiovascular disease, according to family history of hypertension, presence of obesity, inactivity, and consumption of high-fat meat. The plasma renin activity and aldosterone level were described as similar or low in offspring of hypertensive parents,13 14 and in our study the values did not differ between groups. Also, the uric acid level was similar in both groups. In conclusion, young, lean normotensive subjects with a positive history of hypertension show alterations in lipid metabolism, suggesting a positive correlation between lipid metabolism and hypertension heredity.

Received March 17, 1997; first decision April 30, 1997; accepted May 19, 1997.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Hopkins PN, Hunt SC, Wu LL, Williams GH, Williams RR. Hypertension, dyslipidemia, and insulin resistance: links in a chain or spokes on a wheel? Curr Opin Lipid. 1996;7:241-253.[Medline] [Order article via Infotrieve]

2. Julius S, Jamerson K, Mejia A, Krause L, Schork N, Jones K. The association of borderline hypertension with target organ changes and higher coronary risk. JAMA. 1990;264:354-358.[Abstract/Free Full Text]

3. Williams RR, Hunt SC, Hopkins PN, Wu LL, Hasstedt SJ, Berry TD, Barlow GK, Stults BM, Schumacher MC, Ludwig EH, Elbein SC, Wilson DE, Lifton RP, Lalouel JM. Genetic basis of familiar dyslipidemia and hypertension: 15-year results from Utah. Am J Hypertens. 1993;6(11 pt 2):319S-327S.

4. Hinunelmann A, Svensson A, Hansson L. Five-year follow-up of blood pressure and left ventricular mass in children with different maternal histories of hypertension: the Hypertension in Pregnancy Offspring Study. J Hypertens. 1994;12:89-95.[Medline] [Order article via Infotrieve]

5. Grunfeld B, Balzareti M, Romo M, Gimenez M, Gutman R. Hyperinsulinemia in normotensive offspring of hypertensive parents. Hypertension. 1994;23(suppl I):I-12-I-15.

6. Neutel JM, Smith DHG, Graettinger WF, Winer RL, Weber MA. Metabolic characteristics of hypertension: importance of positive family history. Am Heart J. 1993;126:924-929.[Medline] [Order article via Infotrieve]

7. Lopes HF, Silva VF, Giorgi DMA, Bemardes Silva H, Consolim FM, Barreto JA, Krieger EM. Sustained blood pressure elevation in young normotensive with a family history of hypertension. Hypertension. 1995;25:1382. Abstract.

8. SAS Institute Inc. SAS/STAT User’s Guide, Version 6. 4th ed, vol 2. Cary, NC: SAS Institute Inc; 1989.

9. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, Fuchs Z. Hyperinsulinemia: a link between hypertension, obesity and glucose intolerance. J Clin Invest. 1985;75:809-817.[Medline] [Order article via Infotrieve]

10. Ferrari P, Weidmann P, Shaw S, Giachino D, Riesen W, Allemann Y, Heynen G. Altered insulin sensitivity, hyperinsulinemia, and dyslipidemia in individuals with a hypertensive parent. Am J Med. 1991;91:589-596.[Medline] [Order article via Infotrieve]

11. Facchini F, Chen IYD, Clinkingbeard C, Jeppesen J, Reaven GM. Insulin resistance, hyperinsulinemia, and dyslipidemia in nonobese individuals with a family history of hypertension. Am J Hypertens. 1992;5:694-699.[Medline] [Order article via Infotrieve]

12. Ellison RC. Should physicians intervene during childhood to prevent adult hypertension? Schweiz Med Wochenschr. 1995;125:264-269.[Medline] [Order article via Infotrieve]

13. van Hooft IMS, Grobbee DE, Derkx FHM, de Leeuw PW, Schalekamp MADH, Hofman A. Renal hemodynamics and the renin-angiotensin-10 aldosterone system in normotensive subjects with hypertensive and normotensive parents. N Engl J Med. 1991;324:1305-1311.[Abstract]

14. Bianchetti MG, Beretta-Piccoli C, Ferrier C. Blood pressure control in normotensive members of hypertensive families. Kidney Int. 1986;29:882-888.[Medline] [Order article via Infotrieve]




This article has been cited by other articles:


Home page
HypertensionHome page
H. F. Lopes, L. A. Bortolotto, C. Szlejf, C. S. Kamitsuji, and E. M. Krieger
Hemodynamic and Metabolic Profile in Offspring of Malignant Hypertensive Parents
Hypertension, September 1, 2001; 38(3): 616 - 620.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lopes, H. F.
Right arrow Articles by Krieger, E. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lopes, H. F.
Right arrow Articles by Krieger, E. M.